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| | <!-- THIS IS WHERE YOUR MAIN BODY GOES --> | | <!-- THIS IS WHERE YOUR MAIN BODY GOES --> |
| - | <h1> MODELLING </h1> <br> <br> | + | <h1> P2A </h1> <br> <br> |
| - | <p> Our modelling in this project has several aims: </p> | + | <p>This is derived from the Porcine |
| - | <ul type="circle">
| + | |
| - | <li>To find the amount of DPP-IV reduction reached when the system reaches equilibrium</li>
| + | |
| - | <li>To find a way to control the level of DPP-IV reduction</li>
| + | |
| - | <li>To find the minimum number of RdRps, replicons, etc to be initially transfected into the cell, which are required to achieve a steady state for the system</li>
| + | |
| - | <li>To find out how long does it take for the system to reach equilibrium</li>
| + | |
| - | <li>To find out the level of reduction we need to treat diabetes</li>
| + | |
| - | <li>To find out how stable the system is (i.e. will the system only work in very specific situations, or in lots of different systems?)
| + | |
| - | </ul>
| + | |
| - | <p> We are currently using Simbiology in Matlab and Copasi to model the system. We are currently adapting several different models, which come from research into HCV replicons, to our system. If our models can be made to fit our experiments well, we may extend our project to try and find a way to control the level of DPP-IV which is reduced. In addition modelling the system will allow it to be better optimised in the future, and optimum values for constants such as the strength of the ribosome binding sites, and the number of siRNAs produced by each degradation, so that the effect of our biobrick can be optimised. </p>
| + | |
| - | <p> We are currently using Simbiology in Matlab and Copasi to model the system. We are currently adapting several different models, which come from research into HCV replicons, to our system. If our models can be made to fit our experiments well, we may extend our project to try and find a way to control the level of DPP-IV which is reduced. In addition modelling the system will allow it to be better optimised in the future, and optimum values for constants such as the strength of the ribosome binding sites, and the number of siRNAs produced by each degradation, so that the effect of our biobrick can be optimised. </p>
| + | |
| | | | |
| - | <p> Initially we determined that our system should reach some equilibrium after a certain amount of time. This is because firstly, HCV is a successful virus, so the replicons should not completely degrade away as time goes to infinity. Secondly, since there are only a finite amount of resources within the cell, the number of replicons in the system cannot keep increasing forever. This means either the number of replicons must tend towards a certain constant (constant with respect to time), or the number of replicons should tend towards oscillations. </p>
| + | Teschovirus-1 genome and cleaves with high |
| | | | |
| - | <p>
| + | efficiency and leaving no scar following the |
| - | \begin{eqnarray}
| + | |
| - | \label{system1}
| + | formation of a polyprotein MS2 coat protein, |
| - | \frac{dm}{dt} &=& \alpha_m - \beta_m m - k_s ms
| + | |
| - | \\ \label{system2}
| + | P2A and RdRp. This is required as the HCV |
| - | \frac{ds}{dt} &=& \alpha_s - \beta_s s - p_s k_s ms - k_r sr
| + | |
| - | \\ \label{system3}
| + | genome which has one open reading frame |
| - | \frac{dr}{dt} &=& \alpha_r - \beta_r r - p_r k_r sr
| + | |
| - | \end{eqnarray}
| + | from which one long polyprotein is produced. |
| - | </p> | + | |
| | + | RdRp is the final protein in this polygenic |
| | + | |
| | + | mRNA and hence does not have a start codon, |
| | + | |
| | + | adding a start codon could be disastrous for |
| | + | |
| | + | the function of RdRp.</p> |
| | + | |
| | + | <h2> Click <a href="http://parts.igem.org/wiki/index.php?title=Part:BBa_K1442039">here</a> to learn about our P2A. </h2> |
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| | </div> | | </div> |
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